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David J. Baylink - One of the best experts on this subject based on the ideXlab platform.
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Fluoride Therapy for the vertebral crush fracture syndrome
Annals of Internal Medicine, 2020Co-Authors: Robert P Heaney, David J. Baylink, Timothy M. Murray, Pierre J. Meunier, Conrad C Johnston, Joseph L Melton, Charles Nagant De DeuxchaisnesAbstract:Excerpt Fluoride has been proposed as a Therapy for the vertebral crush fracture syndrome for many years; such proposals have been based largely on the well-characterized syndrome of Fluoride intox...
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Fluoride pharmacokinetics in good and poor responders to Fluoride Therapy.
Journal of Bone and Mineral Research, 2010Co-Authors: M E Kraenzlin, S M Farley, C. Kraenzlin, Robert J. Fitzsimmons, David J. BaylinkAbstract:In this study, the relationship between Fluoride pharmacokinetics and the response in spinal bone density to Fluoride treatment was studied in 14 patients with primary osteoporosis treated with Fluoride for at least 1 year. Serum concentrations and urinary excretion of Fluoride were determined after ingestion of 10 mg Fluoride as monofluorophosphate. The pharmacokinetic parameters were calculated according to a linear one-compartment open model. The fasting serum Fluoride level was 8.8 +/- 0.98 mumol/liter. The peak serum Fluoride level was 20.5 +/- 1.4 mumol/liter and was reached within 2 h after ingestion of Fluoride. When the patients were divided into good and poor responders, based on whether they did or did not exhibit a change in spinal bone density of 13 mg/cc per year or more, we found that good responders had decreased renal Fluoride clearance (-62 +/- 13%, p less than .02), increased maximum change in serum Fluoride (+38 +/- 18%, p less than .01), increased extrarenal clearance (+62 +/- 57%, p less than .05) and increased change in serum alkaline phosphatase (ALP) (+241 +/- 169%, p less than 0.02) compared with poor responders. Our data suggest that one factor accounting for a good response is a relatively high serum level of Fluoride. However, although the maximum change in serum Fluoride was greater in good responders compared with poor responders, variations in Fluoride levels could not explain all of the variation in spinal bone density. Therefore, we propose that in addition to differences in serum Fluoride, other factors are also responsible for the good response.
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Incidence of hip fractures in osteoporotic women treated with sodium Fluoride.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2009Co-Authors: B. Lawrence Riggs, M. Kleerekoper, David J. Baylink, Joseph M. Lane, L. Joseph Melton, Pierre J. MeunierAbstract:It has been suggested recently that, although Fluoride Therapy may decrease the occurrence of vertebral fractures, it could increase the risk of hip fractures. To evaluate this possibility, we combined retrospective data from five medical centers that have had a large experience with this therapeutic regimen. In 416 osteoporotic patients who were followed for more than 1,000 patient-years of Fluoride treatment, there were 17 nontraumatic hip fractures. This incidence of 1.6% per year is similar to the incidence, 1.9% per year, for 120 of the patients in this series who had been followed prospectively for 3 years prior to initiation of Fluoride Therapy. The expected incidence for women of the same age in the general community is 0.5% per year. Thus, untreated osteoporotic women are at increased risk for hip fracture, but treatment with Fluoride seems neither to decrease nor to increase the incidence of hip fracture substantially.
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Fluoride Therapy for Osteoporosis
Osteoporosis, 2001Co-Authors: K.-h. William Lau, David J. BaylinkAbstract:Publisher Summary Like all trace elements, Fluoride demonstrates biphasic actions in the organism; intakes below the recommended daily dose result in growth and development retardation, while high intakes, such as those associated with long exposure to Fluoride from endemic or industrial sources, result in skeletal sclerosis. Pharmacologic doses, 20 to 100 mg/day, cause significant increases in skeletal mass. These observations, along with the recognition that the consequences of osteopenia could be reduced in people who had been exposed to Fluoride, led to the suggestion that Fluoride could be of therapeutic value in osteoporosis. This chapter reviews and discusses the clinical use of Fluoride for established osteoporosis. Fluoride is the only orally active bone formation agent in clinical trials. It causes a large increase in spinal bone density, which is needed to restore bone density to a normal within a reasonable time frame. It increases bone formation at trabecular, as well as corticalendosteal, bone sites, which are sites of bone loss in osteoporosis, and it does not increase bone resorption. Moreover, Fluoride acts through a unique mechanism—it inhibits a specific osteoblastic Fluoride-sensitive PTP, which leads to potentiation of the osteogenic actions of endogenous bone cell growth factors. Thus, Fluoride, in effect, may be considered an inexpensive, orally active, bone-specific growth factor Therapy. Accordingly, Fluoride Therapy would be an attractive anabolic Therapy for established osteoporosis. On the other hand, Fluoride treatment has several undesirable side effects that significantly reduce its benefit-to-risk profile and, thereby, diminish its therapeutic value. Although most of the side effects of Fluoride Therapy are manageable, two of these side effects, that is, calcium deficiency and high Fluoride deposition, could have detrimental effects on the architectural integrity and mechanical strength of the bone. Consequently, Fluoride Therapy is a highly controversial Therapy for osteoporosis.
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chapter 48 Fluoride Therapy of established osteoporosis
The Aging Skeleton, 1999Co-Authors: K William H Lau, David J. BaylinkAbstract:This chapter reviews and discusses the clinical use of Fluoride for established osteoporosis. It discusses the current information regarding the molecular mechanism of the action of Fluoride, and the advantages and disadvantages of Fluoride Therapy. It has been well recognized for decades that Fluoride has both beneficial and detrimental effects on the skeleton. On one hand, it is well documented that Fluoride is a bone cell-specific, anabolic agent that effectively stimulates cancellous bone formation and increases spinal bone density without an increase in bone resorption. On the other hand, studies have also demonstrated that Fluoride may cause calcium deficiency and osteomalacia, which reduces the integrity of bone, and that high bone deposition of Fluoride could greatly reduce the biomechanical properties and strength of the skeleton. These undesirable side effects, together, significantly reduce the benefit-to-risk profile of Fluoride Therapy and thereby diminish its therapeutic values. However, at present, Fluoride is the only orally active, bonespecific, anabolic agent that increases bone formation and bone density at appropriate skeletal sites, that is, trabecular and cortical–endosteal bone sites.
S M Farley - One of the best experts on this subject based on the ideXlab platform.
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Fluoride pharmacokinetics in good and poor responders to Fluoride Therapy.
Journal of Bone and Mineral Research, 2010Co-Authors: M E Kraenzlin, S M Farley, C. Kraenzlin, Robert J. Fitzsimmons, David J. BaylinkAbstract:In this study, the relationship between Fluoride pharmacokinetics and the response in spinal bone density to Fluoride treatment was studied in 14 patients with primary osteoporosis treated with Fluoride for at least 1 year. Serum concentrations and urinary excretion of Fluoride were determined after ingestion of 10 mg Fluoride as monofluorophosphate. The pharmacokinetic parameters were calculated according to a linear one-compartment open model. The fasting serum Fluoride level was 8.8 +/- 0.98 mumol/liter. The peak serum Fluoride level was 20.5 +/- 1.4 mumol/liter and was reached within 2 h after ingestion of Fluoride. When the patients were divided into good and poor responders, based on whether they did or did not exhibit a change in spinal bone density of 13 mg/cc per year or more, we found that good responders had decreased renal Fluoride clearance (-62 +/- 13%, p less than .02), increased maximum change in serum Fluoride (+38 +/- 18%, p less than .01), increased extrarenal clearance (+62 +/- 57%, p less than .05) and increased change in serum alkaline phosphatase (ALP) (+241 +/- 169%, p less than 0.02) compared with poor responders. Our data suggest that one factor accounting for a good response is a relatively high serum level of Fluoride. However, although the maximum change in serum Fluoride was greater in good responders compared with poor responders, variations in Fluoride levels could not explain all of the variation in spinal bone density. Therefore, we propose that in addition to differences in serum Fluoride, other factors are also responsible for the good response.
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the increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued
Osteoporosis International, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p<0.03), at a rate that was comparable to the rate of the previous gain that had occurred during the treatment with Fluoride (i.e. −3.23±2.39 mg/cm3 per month, compared with +3.91±1.96 mg/cm3 per month in this subgroup of patients,p<0.001). Although 9 of the 44 subjects showed continuing increases in spinal bone density after discontinuation of the Fluoride Therapy, spinal bone density decreased in the entire group of 44 at an average rate of −1.02±4.72 mg/cm3 per month (p<0.001, compared with the rate of the previous gain during the treatment with Fluoride; i.e. +3.83±1.82 mg/cm3 per month). Surprisingly, our data showed that the rate of decrease in spinal bone density during the post-Fluoride period was not affected by concurrent (undesigned) treatment with calcium, calcium plus estrogen, or calcium plus calcitriol. The cessation of Fluoride Therapy was also associated with a decrease in serum alkaline phosphatase activity (i.e. a decrease from the elevated levels that were observed during the period of Fluoride Therapy, back to the original, pre-treatment levels;p<0.001), and that the rate of spinal bone loss after cessation of Fluoride could be correlated with the prior rate of increase in serum alkaline phosphatase activity that had occurred during the treatment with Fluoride (n=44,r=0.312,p=0.039). Together, the observations from this retrospective analysis of data obtained from our clinical subjects suggest that Fluoride-treated osteoporotic subjects who have exhibited increases in trabecular spinal bone density are at risk for bone loss after discontinuation of the Fluoride Therapy.
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The increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued.
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p
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Evidence that Fluoride Therapy increases trabecular bone density in a peripheral skeletal site.
The Journal of clinical endocrinology and metabolism, 1993Co-Authors: H. Resch, S M Farley, Cesar Libanati, P. Bettica, Eloy E. Schulz, David J. BaylinkAbstract:We measured the spinal bone density (SBD) and femoral condyle bone density (FCD) in normal and osteoporotic females (n = 219) both before and during Fluoride Therapy. SBD and FCD in untreated osteoporotics were significantly lower (P < 0.05) than those in the age-matched controls. SBD and FCD were correlated in the untreated (r = 0.62; P < 0.0001) as well as in the Fluoride-treated osteoporotics (r = 0.42; P < 0.0001). SBD and FCD were significantly increased (P < 0.05) in response to Fluoride Therapy. The average rates of increase in FCD and SBD were similar (1.3 +/- 1.3 vs. 1.24 +/- 1.4 mg/cc.month). We conclude that the osteogenic action of Fluoride is not limited to the axial skeleton. An increase in trabecular bone density also occurs at peripheral weight-bearing sites such as the femoral condyle.
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis International, 1992Co-Authors: S M Farley, Jon E. Wergedal, C R Libanati, E E Schulz, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, J. R. Farley, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT). Spinal bone density increased with time on Fluoride, but the relationship was hyperbolic ( r =0.99, p
Cesar Libanati - One of the best experts on this subject based on the ideXlab platform.
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the increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued
Osteoporosis International, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p<0.03), at a rate that was comparable to the rate of the previous gain that had occurred during the treatment with Fluoride (i.e. −3.23±2.39 mg/cm3 per month, compared with +3.91±1.96 mg/cm3 per month in this subgroup of patients,p<0.001). Although 9 of the 44 subjects showed continuing increases in spinal bone density after discontinuation of the Fluoride Therapy, spinal bone density decreased in the entire group of 44 at an average rate of −1.02±4.72 mg/cm3 per month (p<0.001, compared with the rate of the previous gain during the treatment with Fluoride; i.e. +3.83±1.82 mg/cm3 per month). Surprisingly, our data showed that the rate of decrease in spinal bone density during the post-Fluoride period was not affected by concurrent (undesigned) treatment with calcium, calcium plus estrogen, or calcium plus calcitriol. The cessation of Fluoride Therapy was also associated with a decrease in serum alkaline phosphatase activity (i.e. a decrease from the elevated levels that were observed during the period of Fluoride Therapy, back to the original, pre-treatment levels;p<0.001), and that the rate of spinal bone loss after cessation of Fluoride could be correlated with the prior rate of increase in serum alkaline phosphatase activity that had occurred during the treatment with Fluoride (n=44,r=0.312,p=0.039). Together, the observations from this retrospective analysis of data obtained from our clinical subjects suggest that Fluoride-treated osteoporotic subjects who have exhibited increases in trabecular spinal bone density are at risk for bone loss after discontinuation of the Fluoride Therapy.
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The increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued.
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p
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Evidence that Fluoride Therapy increases trabecular bone density in a peripheral skeletal site.
The Journal of clinical endocrinology and metabolism, 1993Co-Authors: H. Resch, S M Farley, Cesar Libanati, P. Bettica, Eloy E. Schulz, David J. BaylinkAbstract:We measured the spinal bone density (SBD) and femoral condyle bone density (FCD) in normal and osteoporotic females (n = 219) both before and during Fluoride Therapy. SBD and FCD in untreated osteoporotics were significantly lower (P < 0.05) than those in the age-matched controls. SBD and FCD were correlated in the untreated (r = 0.62; P < 0.0001) as well as in the Fluoride-treated osteoporotics (r = 0.42; P < 0.0001). SBD and FCD were significantly increased (P < 0.05) in response to Fluoride Therapy. The average rates of increase in FCD and SBD were similar (1.3 +/- 1.3 vs. 1.24 +/- 1.4 mg/cc.month). We conclude that the osteogenic action of Fluoride is not limited to the axial skeleton. An increase in trabecular bone density also occurs at peripheral weight-bearing sites such as the femoral condyle.
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1992Co-Authors: S M Farley, Jon E. Wergedal, Cesar Libanati, Eloy E. Schulz, John R. Farley, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT).
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Fluoride Therapy for osteoporosis a review of dose response duration of treatment and skeletal sites of action
Calcified Tissue International, 1991Co-Authors: B A Duresmith, S M Farley, Cesar Libanati, M E Kraenzlin, Eloy Schulz, David J. BaylinkAbstract:Osteoporosis is a disease characterized by a reduction in bone density which predisposes to fracture after even minimal trauma. Fluoride, because it has consistently been shown to stimulate bone formation and increase trabecular bone density, has been widely studied for the treatment of osteoporosis. The article focuses on the dose response, duration of treatment, and skeletal sites of action of Fluoride; we also include comments on the effect of Fluoride on vertebral and appendicular fracture rates. The skeletal response to Fluoride doses, ranging from 15 to 43 mg elemental Fluoride per day, included a linear increase in spinal bone density at an average rate of 1.25±0.91 mg/cm3 per month. The rate of increase in spinal bone density was related to the dose of Fluoride (r=0.34,P<0.03). Spinal bone density had increased above the fracture threshold in 44% of patients treated with Fluoride for 32±10 months. The time required to achieve this goal was, however, influenced by the pretreatment spinal bone density and interpatient variation in response to Fluoride treatment. Patients whose spinal bone density remained below the fracture threshold had lower pretreatment bone densities and/or slower rates of increase in spinal bone density (P<0.001). The osteogenic effect of Fluoride was not limited to the spine. After 2 years of Fluoride Therapy, we found bone density in the femoral condyle (measured by QCT) to have increased by 13±2.6 mg/cm3 (n=38,P<0.001); bone density in the hip (measured by DPA) was increased by 0.0261±0.015 g/cm2 (n=55,P<0.025). The efficacy of Fluoride Therapy to reduce fractures is not well established. Recently, investigators from the Mayo Clinic and Henry Ford Hospital reported Fluoride had no effect on the vertebral fracture rate despite a significant increase in spinal bone density, but this finding has not been supported by findings in other studies. Moreover, our preliminary analysis of over 500 Fluoride-treated patients found a time-dependent decrease in vertebral fracture rate related to a corresponding increase in spinal bone density. We conclude that these data, together with the many other positive international findings related to Fluoride, justify continued investigation of this potent agent for the treatment of osteoporosis.
J R Talbot - One of the best experts on this subject based on the ideXlab platform.
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the increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued
Osteoporosis International, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p<0.03), at a rate that was comparable to the rate of the previous gain that had occurred during the treatment with Fluoride (i.e. −3.23±2.39 mg/cm3 per month, compared with +3.91±1.96 mg/cm3 per month in this subgroup of patients,p<0.001). Although 9 of the 44 subjects showed continuing increases in spinal bone density after discontinuation of the Fluoride Therapy, spinal bone density decreased in the entire group of 44 at an average rate of −1.02±4.72 mg/cm3 per month (p<0.001, compared with the rate of the previous gain during the treatment with Fluoride; i.e. +3.83±1.82 mg/cm3 per month). Surprisingly, our data showed that the rate of decrease in spinal bone density during the post-Fluoride period was not affected by concurrent (undesigned) treatment with calcium, calcium plus estrogen, or calcium plus calcitriol. The cessation of Fluoride Therapy was also associated with a decrease in serum alkaline phosphatase activity (i.e. a decrease from the elevated levels that were observed during the period of Fluoride Therapy, back to the original, pre-treatment levels;p<0.001), and that the rate of spinal bone loss after cessation of Fluoride could be correlated with the prior rate of increase in serum alkaline phosphatase activity that had occurred during the treatment with Fluoride (n=44,r=0.312,p=0.039). Together, the observations from this retrospective analysis of data obtained from our clinical subjects suggest that Fluoride-treated osteoporotic subjects who have exhibited increases in trabecular spinal bone density are at risk for bone loss after discontinuation of the Fluoride Therapy.
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The increase in spinal bone density that occurs in response to Fluoride Therapy for osteoporosis is not maintained after the Therapy is discontinued.
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1996Co-Authors: J R Talbot, S M Farley, Cesar Libanati, John R. Farley, M Fischer, A Tabuenca, David J. BaylinkAbstract:In 44 osteoporotic subjects who had been treated with Fluoride for 37±16 months, the Fluoride was discontinued because they had shown Fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the Fluoride Therapy (i.e. 19±9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44,p
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis International, 1992Co-Authors: S M Farley, Jon E. Wergedal, C R Libanati, E E Schulz, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, J. R. Farley, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT). Spinal bone density increased with time on Fluoride, but the relationship was hyperbolic ( r =0.99, p
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1992Co-Authors: S M Farley, Jon E. Wergedal, Cesar Libanati, Eloy E. Schulz, John R. Farley, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT).
M. M. Goette - One of the best experts on this subject based on the ideXlab platform.
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis International, 1992Co-Authors: S M Farley, Jon E. Wergedal, C R Libanati, E E Schulz, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, J. R. Farley, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT). Spinal bone density increased with time on Fluoride, but the relationship was hyperbolic ( r =0.99, p
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Spinal fractures during Fluoride Therapy for osteoporosis: Relationship to spinal bone density
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteopor, 1992Co-Authors: S M Farley, Jon E. Wergedal, Cesar Libanati, Eloy E. Schulz, John R. Farley, J R Talbot, G. N. Javier, L. Lindegren, M. Bock, M. M. GoetteAbstract:Recent studies report that Fluoride Therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of Fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with Fluoride 30±8 mg/day (mean±SD) (equivalent to 66±17 mg NaF/day) and calcium 1500 mg/day for 28±18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT).